ArticleeLife2021
3'HS1 CTCF binding site in human β-globin locus regulates fetal hemoglobin expression.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- Genetic Polymorphisms Associated with Fetal Hemoglobin (HbF) Levels and F-Cell Numbers: A Systematic Review of Genome-Wide Association Studies.International journal of molecular sciences · 2024Pooled it
- New Gene Therapy Strategy for β-Thalassemia.Stem cell reviews and reports · 2026Review
- Single-cell transcriptomics reveals heterocellular γ-globin gene expression in Aγδβ-thalassemia.Blood advances · 2026Article
- MAZ regulates fetal hemoglobin repression by activating MYB transcription.Scientific reports · 2025Article
- Structural variants in the 3D genome as drivers of disease.Nature reviews. Genetics · 2025Review
- Reactivation of developmentally silenced globin genes through forced linear recruitment of remote enhancers.Blood · 2025Article
- Unraveling the Complex Genomic Interplay of Sickle Cell Disease Among the Saudi Population: A Case-Control GWAS Analysis.International journal of molecular sciences · 2025Article
- CTCF is selectively required for maintaining chromatin accessibility and gene expression in human erythropoiesis.Genome biology · 2025Article
- Upregulation of miR‑6747‑3p affects red blood cell lineage development and induces fetal hemoglobin expression by targeting BCL11A in β‑thalassemia.Molecular medicine reports · 2025Article
- CRISPR technology in human diseases.MedComm · 2024Review
- C2H2 Zinc Finger Transcription Factors Associated with Hemoglobinopathies.Journal of molecular biology · 2024Review
- Mutant NPM1 Hijacks Transcriptional Hubs to Maintain Pathogenic Gene Programs in Acute Myeloid Leukemia.Cancer discovery · 2023Article
- Review
- Comprehensive analysis and accurate quantification of unintended large gene modifications induced by CRISPR-Cas9 gene editing.Science advances · 2022Article
- Limitations of mouse models for sickle cell disease conferred by their human globin transgene configurations.Disease models & mechanisms · 2022Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Mutations in the adult β-globin gene can lead to a variety of hemoglobinopathies, including sickle cell disease and β-thalassemia. An increase in fetal hemoglobin expression throughout adulthood, a condition named hereditary persistence of fetal hemoglobin (HPFH), has been found to ameliorate hemoglobinopathies. Deletional HPFH occurs through the excision of a significant portion of the 3' end of the β-globin locus, including a CTCF binding site termed 3'HS1. Here, we show that the deletion of this CTCF site alone induces fetal hemoglobin expression in both adult CD34+ hematopoietic stem and progenitor cells and HUDEP-2 erythroid progenitor cells. This induction is driven by the ectopic access of a previously postulated distal enhancer located in the
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.